BACKGROUND: 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.
METHODS: 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.
METHODS: This patient was ultimately diagnosed with acute pontine cerebral infarction.
METHODS: He received aspirin, clopidogrel, and butylphthalide, as well as acupuncture and Chinese herbal medicine.
RESULTS: After 10 days of treatment, the patient\'s paralysis of the eye muscles improved significantly.
CONCLUSIONS: 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.

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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.

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METHODS: 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.
CONCLUSIONS: 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.
UNASSIGNED: KRANKHEITSBILD: Zu einem „Klick-Phänomen“ kommt es beim forcierten Überwinden einer erworbenen mechanischen Einschränkung der Hebung in Adduktion beim Auge bzw. Strecken des Fingers/Daumens bei der Hand. Die gemeinsame Ursache ist ein Knoten: Beim Auge hinter der Trochlea; der Hand vor dem Ringband A1. Wobei es zu dem „Klick“ über den gleichen Pathomechanismus kommt.
UNASSIGNED: Aufgrund dieser identischen Befunde beim Auge und der Hand kann bei kleinen Kindern angenommen werden, dass die durch Studien bei der Hand bei Neugeborenen und kleinen Kindern mit einem „Trigger thumb/finger“ gewonnenen Erkenntnisse auch auf die Situation beim Auge zutreffen: 1. Im frühen Kindesalter kommt es zu dieser Motilitätsstörung nicht kongenital. Hierzu kommt es höchstwahrscheinlich durch bei der Geburt noch nicht voll entwickelte Gleitverhältnisse, die für eine glatte Passage der Sehne durch die Trochlea/das Ringband A1 erforderlich sind. 2. Bei dieser Motilitätsstörung muss zwischen den Stadien 0–3 unterschieden werden: Stadium 0 = keine Einschränkung der Motilität und kein „Klick-Phänomen“ mehr; Stadium 1 = forciert aktiv; Stadium 2 = nur passiv Strecken/Hebung möglich – mit jeweils einem „Klick-Phänomen“; Stadium 3 = kein Strecken/Hebung möglich und kein „Klick-Phänomen“. 3. Bei den meisten frühkindlichen Fällen kommt es ohne Therapie (75 % nach 6 bis 7 Jahren) zu einer spontanen vollständigen Rückbildung: Was beim Auge nur begrenzt durch Motilitätsübungen in Kombination mit einer Sektorokklusion verkürzt werden kann.
UNASSIGNED: Das „Klick-Phänomen“ ist ein Symptom beim Stadium 1 und 2 der erworbenen mechanischen Einschränkung der Hebung in Adduktion bzw. Strecken des Fingers/Daumens. Es ist kein „Syndrom“, nach dem diese Motilitätsstörung bezeichnet werden kann.

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.

Saccadic oscillations (SOs) mostly occur spontaneously, but can be occasionally triggered by various stimuli. To determine clinical characteristics and underlying mechanisms of triggered SOs, we analyzed the clinical features and quantitative eye-movement recordings of six new patients and 10 patients in the literature who exhibited with triggered SOs. Eleven of the 16 patients (69%) had a lesion involving cerebellum and/or brainstem such as cerebellar degeneration, cerebellitis, or cerebellar infarction. The other causes were vestibular migraine (n = 2), multiple sclerosis (n = 1), Krabbe disease (n = 1), and idiopathic (n = 1). Vestibular stimulation was the most common trigger (n = 11, 69%), followed by removal of visual fixation (n = 4, 25%), hyperventilation (n = 1), light (n = 1), and blink (n = 1). The types of triggered SOs were varied which included ocular flutter (n = 13), opsoclonus (n = 3), vertical SOs (n = 2), and macrosaccadic oscillations (n = 1). Three patients exhibited downbeat nystagmus either before (n = 1) or after (n = 2) the onset of SOs. The frequency of triggered SOs ranged from 4 to 15 Hz, and oscillations with smaller amplitudes had higher frequencies and smaller peak velocities. SOs can be triggered by the modulation of unstable saccadic neural networks through vestibular and visual inputs in lesions of the brainstem and cerebellum.

UNASSIGNED: To review the diagnostic protocols of non-strabismic binocular vision anomalies.
UNASSIGNED: We carried out a literature search on published articles of non-strabismic accommodative and vergence anomalies in different international optometry and ophthalmology journals found in the Pubmed, ResearchGate, Google Scholar, and MEDLINE databases.
UNASSIGNED: The diagnostic criteria and normative data from the nine articles selected show discrepancies and variability in methodologies and techniques in the overall assessment of Non-Strabismic Binocular Vision Anomalies (NSBVA). Near point of convergence measurement is the most common assessment, whereas the vergence facility is the least commonly used assessment in terms of evaluating convergence insufficiency. Near point of convergence > 10 cm alone is the most sensitive sign to detect convergence insufficiency in a community set-up but high positive relative accommodation (>3.50D) is the most sensitive sign to diagnose accommodative excess. On the other hand, monocular accommodative facility < 7 CPM has the highest sensitivity to confirm the diagnosis of accommodative infacility. This review also indicates that the more clinical signs that are included in a set of diagnostic criteria, the lower the prevalence rate for that diagnosis.
UNASSIGNED: There is no standardized and diagnostically validated protocol for the assessment of NSBVAs. Variable cutoff values obtained using different methods and the selection of diagnostic criteria by various researchers have led to discrepancies that highlight the need for diagnostic validity of available protocols (combination of tests) for each anomaly. Clinical signs such as positive relative accommodation (PRA) for accommodative excess, near point of convergence (NPC) for convergence insufficiency and monocular accommodative facility (MAF) for accommodative infacility were found to be useful diagnostic signs of these anomalies. Studies should be carried out for accommodative and vergence dysfunctions using proper designs and methods to validate diagnostic criteria for all age groups. Standardization of assessment protocol and cutoff criteria will also aid in calculating prevalence for non-strabismic binocular vision anomalies.

UNASSIGNED: Radiographic horizontal gaze deviation (RHGD) has been identified as a useful finding on computed tomography (CT) that indicates the affected side in supratentorial ischemic stroke; however, it remains unclear whether RHGD is essentially the same phenomenon as physical horizontal gaze deviation (PHGD). To resolve the issue, this study was conducted.
UNASSIGNED: Retrospective analyses were performed for 671 patients with ischemic stroke and 142 controls who were hospitalized and underwent head CT. First, clinical findings were examined to find differences between RHGD-positive and RHGD-negative patients. Second, patients were classified by their stroke mechanisms and/or affected vascular territories. For each subgroup, RHGD was compared with PHGD in frequency. Third, the proportions for patients divided by positivity for PHGD and RHGD were calculated in the subgroups.
UNASSIGNED: Patients with RHGD had PHGD more often than those without. In all stroke subgroups, RHGD was more frequent than PHGD. The frequency difference was prominent in small-artery occlusion (SAO) and posterior inferior cerebellar artery (PICA) stroke. In SAO of the basilar artery pontine perforator, RHGD was positive in 25% and largely contralesionally-directed. In PICA stroke, lesions in the vestibulocerebellum were associated with contralesional RHGD. Moreover, lesions in the lateral medulla also caused RHGD, which was mainly directed to the ipsilesional side. PHGD-positive stroke without RHGD was infrequent, whereas RHGD-positive stroke without PHGD was commonly observed (PICA stroke, 45.9%; other subgroups, 21.1%-27.5%).
UNASSIGNED: RHGD had different characteristics from PHGD; therefore, assessments of both PHGD and RHGD may lead to more accurate diagnoses.

Congenital fibrosis of the extraocular muscles (CFEOM) type 1 is associated with heterozygous missense variants in KIF21A, which encodes a kinesin-like motor protein. Individuals with CFEOM1 have severe paralysis of upgaze and ptosis, resulting in a pronounced chin-up head posture. There can also be limitations of horizontal eye movements. Loss of function of KIF26A, an unconventional kinesin motor protein that lacks ATP-dependent motor activity, has been recently reported to cause a spectrum of congenital brain malformations associated with defects in migration, localization, and growth of excitatory neurons. It has also been associated with megacolon resembling Hirschsprung\'s disease. We report the case of a boy with homozygous loss of function of KIF26A with restricted eye movements, specifically restricted upgaze and downgaze with variable nystagmus and dissociated vertical eye movements. This case represents a congenital cranial dysinnervation disorder, most similar to CFEOM, and is the first report of a congenital cranial dysinnervation disorder caused by a kinesin other than KIF21A.