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Athletes participating in contact sports such as ice hockey are exposed to a high risk of suffering a concussion. We determined whether recent rule changes regulating contact to the head introduced in 2010-11 and 2011-12 have been effective in reducing the incidence of concussion in the National Hockey League (NHL). A league with a longstanding ban on hits contacting the head, the Ontario Hockey League (OHL), was also studied. A retrospective study of NHL and OHL games for the 2009-10 to 2011-12 seasons was performed using official game records and team injury reports in addition to other media sources. Concussion incidence over the 3 seasons analyzed was 5.23 per 100 NHL regular season games and 5.05 per 100 OHL regular season games (IRR 1.04; 95% CI 1.01, 1.50). When injuries described as concussion-like or suspicious of concussion were included, incidences rose to 8.8 and 7.1 per 100 games respectively (IRR 1.23; 95% CI 0.81, 1.32). The number of NHL concussions or suspected concussions was lower in 2009-10 than in 2010-11 (IRR 0.61; 95% CI 0.45, 0.83), but did not increase from 2010-11 to 2011-12 (IRR 1.05; 95% CI 0.80, 1.38). 64.2% of NHL concussions were caused by bodychecking, and only 28.4% of concussions and 36.8% of suspected concussions were caused by illegal incidents. We conclude that rules regulating bodychecking to the head did not reduce the number of players suffering concussions during NHL regular season play and that further changes or stricter enforcement of existing rules may be required to minimize the risk of players suffering these injuries.

Chronic wound infections are of clinical concern as they often lead to high rates of mortality and morbidity. A point-of-care handheld bacterial fluorescence imaging has been designed to detect the auto-fluorescent characteristics of most clinically relevant species of bacteria. This device causes most species of bacteria to exhibit red fluorescence due to the production of exoproduct porphyrins. One of the most significant contributors to the pathogenicity of chronic wounds is the pathogen Pseudomonas aeruginosa, and interestingly, this organism exhibits an additional unique cyan fluorescence signature. There is an over 90% positive predictive value that, when a chronic wound exhibits cyan fluorescence with the bacterial fluorescence imaging device, the wound will harbor P. aeruginosa. This project seeks to understand what genetic factor(s) contribute to the cyan phenotype observed.

Almost two-thirds of patients with giant cell arteritis (GCA) develop ocular symptoms and up to 30% suffer permanent visual loss. We review the three most common mechanisms for visual loss in GCA, describing the relevant ophthalmic arterial anatomy and emphasising how ophthalmoscopy holds the key to a rapid diagnosis. The short posterior ciliary arteries supply the optic nerve head, while the central retinal artery and its branches supply the inner retina. GCA has a predilection to affect branches of posterior ciliary arteries. The most common mechanism of visual loss in GCA is anterior arteritic optic neuropathy due to vasculitic involvement of short posterior ciliary arteries. The second most common cause of visual loss in GCA is central retinal artery occlusion. When a patient aged over 50 years has both anterior ischaemic optic neuropathy and a central retinal artery occlusion, the diagnosis is GCA until proven otherwise, and they should start treatment without delay. The least common culprit is posterior ischaemic optic neuropathy, resulting from vasculitic involvement of the ophthalmic artery and its pial branches. Here, the ophthalmoscopy is normal acutely, but MR imaging of the orbits usually shows restricted diffusion in the optic nerve.

Twelve days later, he noticed weakness in the right side of his face and presented to a community hospital where a noncontrast CT head was normal and he was discharged home with a diagnosis of Bell’s palsy. At this time, he presented again to hospital where he was admitted for investigations. Guillain–Barre syndrome following SARS-CoV-2 vaccination Author Age Sex Vaccine Facial palsy Other cranial Respiratory Symptom onset (days) Limb paresthesias Antibodies Motor Waheed [1] 82 F Pfizer None None None 8-14 Yes ND Areflexia, limb weakness Razok [2] 73 M Pfizer None None None 16-17 NS ND Areflexia, limb weakness Present 45 M AstraZeneca Bilateral R sixth nerve pals None 12 Yes GM1 negative Areflexia, limb weakness Hasan [3] 62 F AstraZeneca None Dysphagia, Dysarthria Yes, ventilated 8 Yes ND Areflexia, limb weakness Bonifacio [4] 66 M AstraZeneca Bilateral Tongue, mouth numbness None 7 Yes Negative Absent R ankle jerk only Bonifacio 43 M AstraZeneca Bilateral Dysphagia, dysgusia, tongue paraesthesia None 11 Yes Negative Areflexia Bonifacio 51 M AstraZeneca Bilateral None None 7 NS GM3 positive, GM4 borderline None Bonifacio 71 F AstraZeneca Bilateral Dysgusia None 12 NS Negative Areflexia, limb weakness Bonifacio 53 M AstraZeneca Bilateral Facial, perioral paraesthesia None 8 Yes ND Areflexia Patel [5] 37 M AstraZeneca None Dysphagia Mild, no ventilation 14 Yes ND Areflexia, limb weakness Nasuelli [6] 59 M AstraZeneca Bilateral None None 10 Yes Negative Areflexia Maramattom [7] 43 F AstraZeneca Bilateral None Yes, ventilated 10 NS ND Areflexia, limb weakness Maramattom 67 F AstraZeneca Bilateral R abducens palsy, bulbar palsy Yes, ventilated 14 Yes Negative Areflexia, limb weakness Maramattom 53 F AstraZeneca Bilateral R face and tongue numbness Yes, ventilated 12 NS Negative Areflexia, limb weakness Maramattom 68 F AstraZeneca Bilateral Facial numbness, bulbar palsy Yes 14 NS Negative Areflexia, limb weakness Maramattom 70 M AstraZeneca Bilateral Bulbar palsy Yes 11 NS ND Areflexia, limb weakness Maramattom 69 F AstraZeneca Bilateral Bulbar palsy, complete ophthalmoplegia None 12 NS ND Areflexia, limb weakness Maramattom 69 F AstraZeneca Bilateral Bulbar palsy Yes 13 NS ND Areflexia, limb weakness Allen [8] 54 M AstraZeneca Bilateral None None 12 Yes Negative None Allen 20 M AstraZeneca Bilateral None None 23 Yes Negative None Allen 57 M AstraZeneca Bilateral Dysarthria None 15 Yes Negative Areflexia, limb weakness Allen 55 M AstraZeneca Bilateral None None 22 Yes Negative None McKean [9] 48 M AstraZeneca Bilateral None None 10 NS Negative Areflexia, limb weakness ND: not done; NS: not specified.

A 66-year-old woman presented to the Emergency Department with shortness of breath and was found to be febrile and tachycardic. When vision blurring persisted, MRI brain with diffusion-weighted imaging (DWI) was performed and showed extensive bilateral areas of T2/FLAIR hyperintensity (Figure 1), consistent with vasogenic edema and posterior reversible encephalopathy syndrome (PRES). Acutely ill patients with COVID-19 are at risk for neurologic complications including stroke, viral meningitis/encephalitis, cerebral venous thrombosis, hypoxic encephalopathy, and demyelinating disease.1 PRES must be included in the differential diagnosis,2 and appropriate neuroimaging in the form of MRI with DWI performed.3 PRES is a result of an incompletely understood process of failed endothelial regulation resulting in cerebral vasogenic edema and was initially described in patients with immunosuppressive drugs, renal insufficiency, or severe hypertension.4 Occipital and parietal lobes are most frequently affected, and symptoms include headache, altered sensorium, seizure, and vision loss.

Alexia without agraphia is a cortical disconnection syndrome which occurs when the visual information cannot reach the angular gyrus, a region in the parietal lobe of the dominant lobe which is involved in language processing and semantic memory critical for reading.1 Input from the occipital cortex of the dominant hemisphere is unavailable as it is directly damaged, producing homonymous hemianopia, while the intact contralateral occipital cortex cannot communicate with the angular gyrus due to the lesioned splenium of the corpus callosum which carries these decussating fibers to the contralateral hemisphere. [...]the patient is able to write but is unable to read a sentence they have just written (Video 1).2 Letter identification may also be impaired, although the patient can match or draw the shape of the letter (Video 2). Visual field testing is also an important part of the examination as homonymous hemianopia, particularly right-sided, interferes with normal saccadic patterns in reading and can produce a word-length effect similar to that seen in alexia.4 Recognition of alexia allows for better understanding of the patient’s experience and allows for the adoption of management strategies such as using pictograms instead of text for shopping lists and use of apps to convert text to speech. Rehabilitation strategies including listening to repetitive word reading with simultaneous display of the text and tactile-kinesthetic training where patients trace letter outlines on their own skin to improve letter recognition have also shown to be beneficial.5 Key Points: 1.

Magnetic resonance imaging was not performed as the differential diagnosis of severe unilateral visual loss without the presence of RAPD and normal retinal examination is very short and includes non-organic visual loss, subtle maculopathies and, very rarely, LHON which is typically accompanied by mild hyperemia and elevation of optic discs and presence of cecocentral scotoma on VF testing. Acute central vision loss with bilateral hyperemia and mild elevation of the optic nerves with peripapillary telangiectasia is a classic presentation of acute LHON1 which is caused by mutation in the mitochondrial genome affecting the electron transport chain and leading to increased generation of intracellular reactive oxygen species. While randomized trial studying idebenone in LHON demonstrated only a trend toward an improved vision, further longitudinal data demonstrated increased proportion of patients with visual recovery and magnitude of recovery with increased treatment duration thus the current recommendation is to start idebenone treatment early and maintain it for 24 months to maximize efficacy.8,9 Corresponding author:

Macular optical coherence tomography (OCT) shows severe thinning and loss of architecture in the inner retina layers (grey arrows) supplied by the retinal circulation (C) with preservation of the outer retina supplied by the choroidal circulation. BRAO is easily missed if patients are not examined in the acute phase when inner retinal edema and whitening is present; however, it is critical to distinguish this entity from optic neuropathies as diagnosis of BRAO necessitates a thorough work-up for embolic sources which should include MRI with diffusion-weighted imaging, MRI or computed tomography (CT) angiography of the entire carotid tree and echocardiography.2 Patients with BRAO are at high risk for ischemic stroke with approximately 25% demonstrating detectable areas of cerebral ischemia on MRI at the time of diagnosis.3 This case emphasizes the critical role of macular OCT in evaluating patients with UVFDss respecting the horizontal midline. All patients with a visual field defect and no evidence of optic neuropathy (optic nerve head pallor and RAPD) should have macular OCT performed which will reveal atrophy of all inner retinal layers in BRAO as compared to selective ganglion cell and nerve fiber layer loss in optic neuropathies.1 Corresponding author:

The first report of tretinoin-induced papilledema was in pediatric patients taking an oral formulation between 50 and 90 mg daily for treatment of acute promyelocytic leukemia, with onset as early as 1 week after initiation.1 Topical tretinoin has been reported to produce intracranial hypertension when taken concurrently with oral doxycycline for 2 months2 but not as a single agent. Tetracyclines have also been reported to alter endothelial cell function and preserve the integrity of the blood–brain barrier in animal models.5 It is not known whether this effect involves RAR signaling pathways; however, anti-inflammatory effects of minocycline have been shown to require retinoids in vitro.6 We suggest that upregulation or sensitization of RARs may occur after exposure to tetracyclines in susceptible individuals and create a dramatic response to even low-dose vitamin A derivatives. Activation of RARα, RARγ, or RXRα increases barrier tightness in human induced pluripotent stem cell-derived brain endothelial cells.

Toxic exposures, including poisoning with methanol, ethylene glycol, carbon monoxide, manganese and cyanide, are also important diagnostic considerations in people with bilateral basal ganglia infarcts.3 4 Carbon monoxide poisoning is relatively common and can present with acute headache, nausea and altered level of consciousness or coma; however, the lack of any affected household members would be against this. Methanol and ethylene glycol, a key ingredient in antifreeze, may be inadvertently or deliberately ingested and present with acute metabolic acidosis and encephalopathy3 Bilateral basal ganglia infarction may also relate to cocaine use.5Box 1 Differential diagnosis of bilateral putaminal infarctions Metabolic disorders (Wilson’s disease, Fahr’s disease, Leigh’s syndrome, glutaric aciduria type 1) Hypoxic-ischaemic encephalopathy Mitochondrial disorders Metabolic acidosis Toxic poisoning (methanol, ethylene glycol, carbon monoxide, cocaine, manganese, cyanide) Liver disease (chronic cirrhosis with portal hypertension, etc) Nonketotic hyperglycaemia Hypoglycaemia Osmotic myelinolysis Neurodegenerative disorders with brain iron accumulation Creutzfeldt-Jakob disease Neuro-Behçet’s disease Question 3: what other entities could present with symmetric bilateral optic neuropathy? The finding of acute bilateral putaminal infarcts at presentation 2 years before and current evidence of bilateral severe symmetric optic neuropathy is very characteristic of methanol toxicity. [...]questioning her use of alcohol, specifically home-brewed varieties, before the onset of visual loss was the most important next step to establish the diagnosis. Vision loss typically occurs 12–48 hours after ingestion because of this delay in formic acid accumulation.8 Histopathological studies show demyelination and vacuolation of retinal ganglion cell axons and oedema of adjacent oligodendrocytes and astroglia.8–10 Methanol toxicity is also associated with isolated bilateral haemorrhagic infarcts in the putamen, which are similarly specifically vulnerable as highly metabolic structures.11 In addition to the direct effect of formic acid on mitochondria, neurotoxicity may also result from hypoperfusion and ischaemia due to metabolic acidosis.12 13 Other possible affected brain regions include the subcortical white matter, globus pallidus and brainstem.14 This patient’s medical records at the time of hospital admission 2 years before had mentioned metabolic acidosis, but this had been attributed to dehydration.