Pearls & Oy-sters: INO Plus From Downward Herniation-A Cautionary Tale Regarding Neuro-Ophthalmologic Signatures of Brainstem Compression.

Pupillary assessment is a quintessential part of the clinical examination in neuro-intensive care patients because it provides insight into the integrity of midbrain reflex arcs. Abnormal pupils, particularly anisocoria and later bilateral fixed mydriasis, are classically used to assess expansive intracranial processes because they are frequently considered early indicators of transtentorial midbrain compression due to elevated intracranial pressure. Complex ocular motor deficits mapping to the midbrain are rarely described in the setting of high transtentorial pressure. This is likely because ocular motor deficits typically occur in conjunction with decreased consciousness and corticospinal tract dysfunction reflecting advanced midbrain compromise. We present a case of left midbrain compression due to downward herniation in a patient with acute-on-chronic bilateral subdural hematoma. Ocular motor assessment demonstrated left internuclear ophthalmoplegia (INO) and an ocular tilt reaction, termed INO plus. However, pupillary, mental status, and sensorimotor examinations were unremarkable. Head magnetic resonance imaging revealed acute perforator ischemia in the left pontomesencephalic tegmentum, localizing to the ipsilateral medial longitudinal fasciculus and graviceptive oculocephalic circuits. Microvascular compromise secondary to mechanical pressure is discussed as a causative mechanism. We caution against overreliance on "telltale pupils" in suspected brainstem compression and recommend checking for other oculomotor signs.

Efficacy of restitutive interventions for oculomotor deficits in adults with mild traumatic brain injury: a systematic review and meta-analysis.

BACKGROUND: Mild traumatic brain injury (mTBI) can cause persistent symptoms suggestive of oculomotor deficits. This research synthesized evidence on restitutive interventions for reducing oculomotor deficits in adults with mTBI to understand if these interventions have clinical utility for improving recovery. METHODS: Medline, EMBASE, CINHAL, PsychInfo, and Scopus, databases were searched for experimental studies published in English. We rated risk of bias (RoB) using recommended tools, and the certainty of the evidence according to GRADE guidelines. We conducted meta-analyses for similar outcomes reported in at least two studies. RESULTS: Out of 5,328 citations, 12 studies (seven case series and five crossover design), with a combined sample size of 354 participants; (43% males) met the inclusion criteria and were analyzed. The analysis revealed a trend toward improvement of oculomotor deficits and visual tasks in response to restitutive intervention. None of the studies addressed sex or gender effects. All studies had high RoB, suggesting low certainty in the reported results. DISCUSSION: Restitutive interventions may be beneficial for adults with oculomotor deficits after mTBI, however overall certainty of the evidence remains low. Future efforts must include enhancing attention to study methodology and reporting, sex and gender analyses, and reaching a consensus on outcome measures. PROSPERO REGISTRATION NUMBER: CRD42022352276.

Neural consequences of symptomatic convergence insufficiency: A small sample study.

INTRODUCTION: Convergence insufficiency (CI) is an oculomotor abnormality characterised by exophoria and inadequate convergence when focusing on nearby objects. CI has been shown to cause symptoms when reading. However, the downstream consequences on brain structure have yet to be investigated. Here, we investigated the neural consequences of symptomatic CI, focusing on the left arcuate fasciculus, a bundle of white matter fibres which supports reading ability and has been associated with reading deficits. METHODS: We compared the arcuate fasciculus microstructure of participants with symptomatic CI versus normal binocular vision (NBV). Six CI participants and seven NBV controls were included in the analysis. All participants were scanned with 3 T magnetic resonance imaging (MRI), and anatomical and diffusion-weighted images were acquired. Diffusion-weighted images were processed with TRACULA to identify the arcuate fasciculus in each participant and compute volume and radial diffusivity (RD). RESULTS: Compared with NBV controls, those with symptomatic CI had significantly smaller arcuate fasciculi bilaterally (left: t = -3.21, p = 0.008; right: t = -3.29, p = 0.007), and lower RD in the left (t = -2.66, p = 0.02), but not the right (t = -0.81, p = 0.44, false discovery rate (FDR)-corrected p > 0.05) arcuate fasciculus. Those with higher levels of reading symptoms had smaller arcuate fasciculi (r = -0.74, p = 0.004) with lower RD (r = -0.61, p = 0.03). CONCLUSIONS: These findings suggest that symptomatic CI may lead to microstructural changes in the arcuate fasciculus. Since it is highly unlikely that abnormalities in the arcuate fasciculus are the cause of the neuromuscular deficits in the eyes, we argue that these changes may be a potential neuroplastic consequence of disruptions in sustained reading.

Convergence insufficiency in patients with post-concussion syndrome is accompanied by a higher symptom load: a cross-sectional study.

OBJECTIVE: To estimate the prevalence of convergence insufficiency (CI) in adult patients with post-concussion syndrome and determine the impact of CI on symptom load. METHODS: Cross-sectional study of 103 patients with neurological symptoms 2-6 months after a concussion. Symptoms were assessed with the Rivermead Post Concussion Symptoms Questionnaire (RPQ), and CI was diagnosed using near point of convergence, vergence facility, and the Convergence Insufficiency Symptom Survey. The RPQ score for patients with and without CI was compared, and sensitivity, specificity, and area under the receiver operating characteristic curve for the two visually related RPQ questions as indicators of CI were calculated. RESULTS: The proportion of patients diagnosed with symptomatic CI was 20.4% (95% confidence interval: 13.1-29.5%). The RPQ score was significantly higher for patients with symptomatic CI both before (p = .01) and after removal of the two visually related questions in the RPQ-questionnaire (p = .03). The two visually related RPQ questions were unable to detect CI. CONCLUSION: In patients with post-concussion syndrome, the load of nonvisual symptoms is higher in the presence of CI. A prospective interventional study on CI is required to study the relationship between CI and other post-concussion symptoms.

Unusual and Rare Causes of Monocular Elevation Deficit.

INTRODUCTION: To study the rare and unusual causes of monocular elevation deficit. METHODS: Five patients presenting to us with diplopia and elevation deficit were thoroughly examined and were found to have monocular elevation deficit due to rare causes. OBSERVATIONS: All five were found to have different underlying etiologies - iatrogenic, sphenoid wing meningioma, cysticercosis, sarcoidosis and mid brain infarct, and were managed appropriately. DISCUSSION: Monocular Elevation Deficit can occur due to a variety of causes. Having a high index of suspicion for the more serious etiologies is of utmost importance. Thorough clinical examination and imaging help clinch the diagnosis.

Pearls & Oy-sters: Ocular Myasthenia Gravis: Central Ocular Motor Signs and Unilateral Visual Loss Caused by the Great Neuro-Ophthalmologic Impersonator.

Myasthenia gravis (MG) has been described as a great mimicker of other neurologic and ocular motility disorders, including centrally mediated ophthalmoplegia. For example, ocular myasthenia gravis (ocular MG) may cause impaired binocular visual acuity for near vision due to reduced accommodation or for distance vision due to accommodative excess. Notably, accommodative excess due to ocular MG is rare, but may occur with exotropia, with or without diplopia. We report 2 cases of ocular MG: First, a 32-year-old man with exotropia, bilateral hypometric and slowed adducting saccades with dissociated abducting nystagmus, miosis, and decreased distance vision in his right eye; second, a 45-year-old man with similar ocular motor deficits, miosis, and myopia. Both patients showed ocular motor deficits which appeared to localize to the pons but were instead due to ocular MG. Ocular MG should be considered in patients who present with reduced visual acuities due to any disruption in accommodation. Any ocular motor deficit, even if appearing to be centrally mediated or occurring without ptosis, may be caused by ocular MG.

Midbrain lesion-induced disconjugate gaze: a unifying circuit mechanism of ocular alignment?

BACKGROUND: Disconjugate eye movements are essential for depth perception in frontal-eyed species, but their underlying neural substrates are largely unknown. Lesions in the midbrain can cause disconjugate eye movements. While vertically disconjugate eye movements have been linked to defective visuo-vestibular integration, the pathophysiology and neuroanatomy of horizontally disconjugate eye movements remains elusive. METHODS: A patient with a solitary focal midbrain lesion was examined using detailed clinical ocular motor assessments, binocular videooculography and diffusion-weighted MRI, which was co-registered to a high-resolution cytoarchitectonic MR-atlas. RESULTS: The patient exhibited both vertically and horizontally disconjugate eye alignment and nystagmus. Binocular videooculography showed a strong correlation of vertical and horizontal oscillations during fixation but not in darkness. Oscillation intensities and waveforms were modulated by fixation, illumination, and gaze position, suggesting shared visual- and vestibular-related mechanisms. The lesion was mapped to a functionally ill-defined area of the dorsal midbrain, adjacent to the posterior commissure and sparing nuclei with known roles in vertical gaze control. CONCLUSION: A circumscribed region in the dorsal midbrain appears to be a key node for disconjugate eye movements in both vertical and horizontal planes. Lesioning this area produces a unique ocular motor syndrome mirroring hallmarks of developmental strabismus and nystagmus. Further circuit-level studies could offer pivotal insights into shared pathomechanisms of acquired and developmental disorders affecting eye alignment.

An unexpected turn: a case of torsional anomalous retinal correspondence after myectomy of previously anteriorized inferior oblique muscles in a child.

We report a case of torsional diplopia caused by presumed torsional anomalous retinal correspondence after myectomy of previously asymmetrically anteriorized inferior oblique muscles for inferior oblique overaction. Given this patient's experience, it may be prudent to operate with caution on previously anteriorized inferior oblique muscles, especially when anteriorization is performed at a very young age.

Sensitivity of Magnetic Resonance Imaging of the Medial Longitudinal Fasciculus in Internuclear Ophthalmoplegia.

BACKGROUND: Internuclear ophthalmoplegia (INO) is a result of insult to the medial longitudinal fasciculus (MLF). Clinicoradiological correlation in patients with INO has been reported to be poor; however, prior studies have used low resolution MRI imaging techniques and included patients with subclinical INO. We aimed to determine the sensitivity of modern MRI interpreted by a specialist neuroradiologist to detect clinically evident INO. METHODS: A retrospective chart review of patients in 2 tertiary University-affiliated neuro-ophthalmology practices with the diagnosis of INO. MRI scans of all patients were reviewed and interpreted by a fellowship-trained neuroradiologist for the presence of lesion in MLF and concordance with the original imaging report. RESULTS: Forty-five patients were included in the study: 33 with demyelinating disease, 11 with stroke, and 1 with intracranial mass. A visible MLF lesion was present in 25/33 demyelinating cases and 7/11 ischemic cases. Lesions in 2 cases in each group were identified only after review by a fellowship-trained neuroradiologist. In demyelinating INO, patients with a visible MLF lesion were more likely to show other brainstem (72%) and supratentorial (51%) white matter lesions. CONCLUSIONS: In 25% of patients with demyelinating INO and 33% of patients with ischemic INO, no visible lesion was identified on current high-quality MRI imaging. Review of imaging by a neuroradiologist increased the possibility of lesion been identified.

Acute bilateral hypotropia and esotropia complex as first manifestation of multiple sclerosis: a case report.

A 21-year-old Japanese woman presented with sudden eye movement disorders. An ophthalmic examination revealed bilateral hypotropia and esotropia complex. Brain magnetic resonance imaging revealed abnormal signals in the posterior and medial part of the lower pontine tegmentum (including periventricular and subcortical white matter) that were suggestive of demyelination. A cerebrospinal fluid test was positive for oligoclonal bands. She was subsequently diagnosed with multiple sclerosis and was administered intravenous methylprednisolone and oral dimethyl fumarate, with complete recovery from hypotropia and esotropia after two months. Bilateral hypotropia and esotropia are important clinical signs for the accurate diagnosis of multiple sclerosis.