We report a 34-year-old male with a previously uninvestigated lifelong blindness of the right eye from compressive optic neuropathy secondary to congenital herniation of the gyrus rectus (HGR). His past medical history was otherwise unremarkable, with no history of prior head or ocular trauma. On examination, he had no light perception in the right eye, right relative afferent pupillary defect (RAPD), and primary optic atrophy. His left eye had normal visual acuity, color vision, and a healthy optic disc. There was a sensory exotropia in the right eye; however, extraocular movements were intact and the remainder of his neurological exam was normal. MRI revealed compression of the prechiasmatic right optic nerve from HGR and atrophy of the right optic nerve and optic chiasm (Figures 1 and 2), without any parenchymal mass lesions. There were no signal abnormalities in the optic nerves or the chiasm.

An 80-year-old man was seen in urgent neuro-ophthalmology consultation for bilateral vision loss. He had a past medical history of hypertension and metastatic stage IV colorectal adenocarcinoma. Four months prior to presentation, he developed gradual onset, painless blurred vision in his right eye. He underwent cataract surgery in that eye, but his vision continued to decline to the point of no light perception. He developed new onset, painless, blurred vision in his left eye 3 weeks prior to presentation and woke up with no light perception in his left eye one day prior to presentation.

Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is a rare progressive maternally inherited mitochondrial disease that clinically harbours various neurological and systemic manifestations.

A 70-year-old woman was seen in neuro-ophthalmology consultation for a progressive right esotropia. She had a past medical history of asthma and osteoporosis, and her ocular history was significant for pathological myopia (spherical equivalent of −23.00 D OD and −21.00 D OS), bilateral cataract surgeries, and laser retinopexy for retinal tears. Twenty-five years prior to presentation, she developed binocular horizontal diplopia and was found to have a limitation of abduction to 60% and 80% of normal in the right and left eyes, respectively, by a previous neuro-ophthalmologist. She developed a progressive maculopathy in the right eye secondary to myopia, resulting in the resolution of double vision. The resolution occurred because the double vision was binocular in nature and the loss of vision in her right eye functioned similar to monocular occlusion. However, she noticed that her right eye continued to turn in toward her nose.

A 65-year-old healthy woman presented with a 15-year history of binocular horizontal diplopia worse when looking left. She had previously been thoroughly investigated multiple times for a left sixth nerve palsy (6NP) 15 years ago and had three normal magnetic resonance imaging (MRI) scans of the brain/orbits with contrast, normal acetylcholine receptor antibodies, normal thyroid function tests, normal cerebrospinal fluid, and normal nerve conduction studies and single-fibre electromyography. She was treated with prism glasses, which resulted in resolution of her symptoms in primary position.

Stroke is relatively rare in children but has become increasingly recognized clinically. Hemiplegic migraine (HM) is a rare subtype of migraine, with attacks typically beginning in childhood or adolescence. Attacks are characterized by migraine headaches and motor weakness, which develop over several minutes. HM may therefore mimic acute stroke; however, symptoms last less than an hour and resolve spontaneously, often without sequela.1–4 Distinction between these entities is important due to their different urgency and management. Neuroimaging is indispensible in working up patients presenting to the Emergency Department with stroke-like symptoms and can be used to distinguish between infarction and HM.

Patients with mechanical heart valves are at high thrombotic risk and require warfarin. Among those developing intracranial hemorrhage, limited data are available to guide clinicians with antithrombotic reinitiation. This 13-patient case series of warfarin-associated intracranial hemorrhages found the time to reinitiate antithrombotic therapy (17 days, interquartile range 21.5 days), and changes to international normalized ratio targets were variable and neither correlated with the type, location, or etiology of bleed, nor the valve and associated thromboembolic risk. The initial presentation significantly impacted prognosis, and diligent assessment and follow-up may support positive long-term outcomes.

A 26-year-old female presented with a complaint of intermittent oscillopsia and binocular vertical diplopia for the past 5 years. Over the past several months, she had noticed intermittent pulsatile tinnitus. She was otherwise healthy with no previous history of trauma and had no other visual or neurologic complaints. In Neuro-ophthalmology clinic, she was found to have 20/15 vision in both eyes with full ocular motility. There was a small exophoria in primary position and small esophoria in downgaze. Her slit lamp and fundus examinations were normal. During the assessment, the left eye was noted to undergo high-frequency, small amplitude incyclotorsional oscillations for a few seconds at a time (Video 1 in the supplementary material), which she was able to provoke by looking down. The diagnosis of superior oblique myokymia was made, and an MRI/MRA of the brain was requested.

This is a case of a 30-year-old right-handed male patient who presented to the hospital in 2014 after hitting his head on the mat during a wrestling match followed by headache and temporary peripheral vision limitation. The patient’s past medical history was unremarkable. On physical examination, Glasgow Coma Scale was 15 with no focal neurological deficits. Unenhanced head computed tomography (CT) and enhanced brain magnetic resonance imaging (MRI) were performed (Figure 1). The patient was managed conservatively, and follow-up CT and MRI in 2015 (Figure 2) demonstrated significant decrease in size of the previously seen right frontoparietal lesion with also changes in its radiological features. The patient remained asymptomatic for about 3 years when in 2018 he presented to the Emergency Department with increasing headaches and peripheral vision loss. MRI demonstrated an increase in the right frontal lesion size (Figure 3). He underwent surgical resection of the lesion.

A 61-year-old male presented to our hospital complaining of claudication: bilateral leg weakness impeding mobility. Symptoms started after 100 m of walk and recede after several minutes of rest. The patient was obese, with a body mass index (BMI) of 41 kg/m2 and reported a weight gain of about 55 pounds in the last year. Patient’s comorbidities were dyslipidemia, hypertension, and antithrombin III deficiency. The patient also suffered from chronic low-back pain recently worsened and cervical pain. Pulses in the lower limbs were present. Neurological examination was also unremarkable.

In traumatic brain injury (TBI), future integration of multimodal monitoring of cerebral physiology and high-frequency signal processing techniques, with advanced neuroimaging, proteomic and genomic analysis, provides an opportunity to explore the molecular pathways involved in various aspects of cerebral physiologic dysfunction in vivo. The main issue with early and rapid discovery in this field of personalized medicine is the expertise and complexity of data involved. This brief communication highlights the CAnadian High-Resolution Traumatic Brain Injury (CAHR-TBI) Research Collaborative, which has been formed from centers with specific expertise in the area of high-frequency physiologic monitoring/processing, and outlines its objectives.