A acute pontine infarction with one-and-a-half syndrome as the manifestation: A case report.

RATIONALE: Sudden ocular dyskinesia is usually associated with ophthalmic diseases and rarely with cerebrovascular diseases. This is a rare case of a patient with a sudden onset of ocular dyskinesia due to occlusion of the anterior inferior cerebellar artery and the spiral modiolar artery. This article describes eye movement disorders associated with cerebrovascular disease, aiming to improve our understanding of cerebrovascular diseases and improve the ability of early diagnosis and differential diagnosis. PATIENT CONCERNS: A 52-year-old man presented with acute pontine cerebral infarction 2 days before presentation. The main symptoms were the inability to adduct and abduct the left eyeball, the ability to abduct but not adduct the right eyeball, and horizontal nystagmus during abduction. Cranial computed tomography in our emergency department suggested cerebral infarction, and magnetic resonance imaging examination after admission confirmed the diagnosis of acute pontine cerebral infarction. DIAGNOSIS: This patient was ultimately diagnosed with acute pontine cerebral infarction. INTERVENTIONS: He received aspirin, clopidogrel, and butylphthalide, as well as acupuncture and Chinese herbal medicine. OUTCOMES: After 10 days of treatment, the patient's paralysis of the eye muscles improved significantly. LESSONS: Eye movement disorders are sometimes an early warning sign of impending vertebrobasilar ischemic stroke. Patients with acute ischemic stroke who have early detection of oculomotor disturbances should be promptly imaged, as missed diagnosis may lead to serious consequences or even death. It provided us with a new diagnostic idea.

A Rare Multinuclear Lesion Secondary to Multifactorial Ischemic Stroke: A Case Report on Eight-and-a-Half Syndrome.

Internuclear ophthalmoparesis (INO) is a horizontal eye movement disorder that is associated with a lesion at the medial longitudinal fasciculus (MLF). One-and-a-half syndrome occurs when the lesion involves the MLF and the ipsilateral abducens nuclei or the paramedian pontine reticular formation (PPRF) in the dorsomedial tegmentum of the pons. When the lesion is large enough, the fascicles of the facial nerve (CNVII) can also be involved, resulting in an ipsilateral facial nerve palsy. In combination with one-and-a-half syndrome, this condition becomes eightand- a- half syndrome (EHS). Here, we describe a unique case of EHS in a 72-year-old male with multiple ischemic stroke risk factors who presented with INO, conjugate gaze palsy, ipsilateral facial palsy, and a transient contralateral hemiparesis. Recognizing this pattern of neurologic deficits improves localization of the lesion, prevents misdiagnosis of Bell's Palsy, and expedites proper treatment.

[Click phenomenon in acquired Jaensch-Brown syndrome and trigger finger/thumb: the Notta syndrome]. / "Klick"-Phänomen beim erworbenen Jaensch-Brown-Syndrom und schnellenden Finger/Daumen: dem Notta-Syndrom.

CLINICAL FEATURES: The click phenomenon occurs when an acquired mechanical restriction of the elevation in adduction of the eye or of the extension of the finger/thumb, is forcefully overcome. The common cause is a nodule either of the superior oblique tendon posterior to the trochlea in the case of a Jaensch-Brown syndrome or of the digital flexor tendon anterior to the A1 annular pulley in the case of a trigger finger. Both locations share similar anatomical conditions for the development of the nodule and the pathomechanism of the click. RESULTS: From these identical findings in the eye and the hand in small children it can be assumed that the results from the studies of the hand in newborns and infants with a trigger thumb/finger are also applicable to the situation of the eye. 1. This motility disorder is not congenital. This is most likely due to an incomplete development at the time of birth of the sliding factors needed for a free passage of the tendon through the trochlea and the A1 annular pulley. 2. A distinction must be made between stages 0-3: stage 0 = no more restriction of the motility and no click phenomenon; stage 1 = forced active extension/elevation possible; stage 2 = only passive extension/elevation, each with a click phenomenon; stage 3 = no extension/elevation possible and no click phenomenon. 3. In most cases in early childhood there is a spontaneous complete recovery (75% after 6-7 years). In the eye this spontaneous course can only limitedly be shortened with motility exercises in combination with segmental occlusion. CONCLUSION: The click phenomenon is a symptom of stages 1 and 2 of an acquired mechanical restriction of the elevation in adduction of the eye or the extension of the finger/thumb. It should not be called a syndrome.

Francisella tularensis Infection Causing Parinaud Oculoglandular Syndrome.

BACKGROUND Parinaud oculoglandular syndrome is a unilateral granulomatous palpebral conjunctivitis associated with preauricular, submandibular, and cervical lymphadenopathies. Several infectious diseases can cause Parinaud oculoglandular syndrome, usually with a conjunctival entry. The most common underlying pathology is cat scratch disease, followed by the oculoglandular form of tularemia. Diagnosis is usually a serious challenge as these infections are themselves rare. On the other hand, Parinaud oculoglandular syndrome may be a rare manifestation of more common disorders (eg, tuberculosis, syphilis, mumps, herpes simplex and Epstein-Barr virus, adenovirus, Rickettsia, Sporothrix, Chlamydia infections). CASE REPORT We present the case of a 66-year-old man with granulomatous conjunctivitis and ipsilateral preauricular, submandibular, and upper cervical lymphadenopathies following a superficial corneal injury. Although the systematic amoxicillin/clavulanic acid and metronidazole antibiotic therapy started immediately at admission, the suppuration of the lymph nodes required surgical drainage. Based on his anamnesis (sheep breeding; a twig scratching his eye 2 days before the initial attendance) and symptoms, a zoonosis, namely the oculoglandular form of tularemia, was suspected, empiric ciprofloxacin therapy was administered, and the patient recovered without sequelae. The Francisella tularensis infection was eventually confirmed by microagglutination serologic assay. CONCLUSIONS If Parinaud oculoglandular syndrome is diagnosed and cat scratch fever as the most common etiology is not likely, other zoonoses, especially the oculoglandular form of tularemia, should be suspected. Serology is the most common laboratory method of diagnosing tularemia. Empiric fluoroquinolone (ciprofloxacin) or aminoglycoside (gentamicin or streptomycin) antibiotic therapy should be started immediately at the slightest suspicion of oculoglandular tularemia.

Oculomotor Dysfunction in Idiopathic and LRRK2-Parkinson's Disease and At-Risk Individuals.

Background: Video-oculography constitutes a highly-sensitive method of characterizing ocular movements, which could detect subtle premotor changes and contribute to the early diagnosis of Parkinson's disease (PD). Objective: To investigate potential oculomotor differences between idiopathic PD (iPD) and PD associated with the G2019S variant of LRRK2 (L2PD), as well as to evaluate oculomotor function in asymptomatic carriers of the G2019S variant of LRRK2. Methods: The study enrolled 129 subjects: 30 PD (16 iPD, 14 L2PD), 23 asymptomatic carriers, 13 non-carrier relatives of L2PD patients, and 63 unrelated HCs. The video-oculographic evaluation included fixation, prosaccade, antisaccade, and memory saccade tests. Results: We did not find significant differences between iPD and L2PD. Compared to controls, PD patients displayed widespread oculomotor deficits including larger microsaccades, hypometric vertical prosaccades, increased latencies in all tests, and lower percentages of successful antisaccades and memory saccades. Non-carrier relatives showed oculomotor changes with parkinsonian features, such as fixation instability and hypometric vertical saccades. Asymptomatic carriers shared multiple similarities with PD, including signs of unstable fixation and hypometric vertical prosaccades; however, they were able to reach percentages of successful antisaccade and memory saccades similar to controls, although at the expense of longer latencies. Classification accuracy of significant oculomotor parameters to differentiate asymptomatic carriers from HCs ranged from 0.68 to 0.74, with BCEA, a marker of global fixation instability, being the parameter with the greatest classification accuracy. Conclusions: iPD and LRRK2-G2019S PD patients do not seem to display a differential oculomotor profile. Several oculomotor changes in asymptomatic carriers of LRRK2 mutations could be considered premotor biomarkers.

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.

Combined diagnosis for Parkinson's disease via gait and eye movement disorders.

BACKGROUND AND OBJECTIVES: With the discovery of the potential role of gait and eye movement disorders in Parkinson's disease (PD) recognition, we intend to investigate the combined diagnostic value of gait and eye movement disorders for PD. METHODS: We enrolled some Chinese PD patients and healthy controls and separated them into the training and validation sets based on enrollment time. Performance in five oculomotor paradigms and in one gait paradigm was examined using an infrared eye tracking device and a wearable gait analysis device. We developed and validated a combined model for PD diagnosis via multivariate stepwise logistic regression analysis. Furthermore, subgroup comparisons and multi-model comparison were performed to assess its applicability and advantages. RESULTS: A total of 145 PD patients and 80 healthy controls in China were recruited. The pro-saccade velocity, the trunk-sway max, and the turn mean angular velocity were finally screened out for the model development. Incorporating age factor, the ternary model demonstrated more satisfactory performance on ROC (AUC of 0.953 in the training set and AUC of 0.972 in the validation set), calibration curve, and decision curve. A nomogram was drawn to visualize the model. The combined model outperforms individual models with a broad application and the unique diagnostic value for early detection of PD patients, especially TD-PD patients. CONCLUSION: We demonstrated the presence of gait and eye movement disorders, as well as the feasibility, applicability, and superiority of employing them together to diagnose PD.

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.

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.

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.

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.

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.