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.

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.

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: Opsoclonus is a rare disorder characterized by conjugate multidirectional, horizontal, vertical, and torsional saccadic oscillations, without intersaccadic interval, resulting from dysfunction within complex neuronal pathways in the brainstem and cerebellum. While most cases of opsoclonus are associated with autoimmune or paraneoplastic disorders, infectious agents, trauma, or remain idiopathic, opsoclonus can also be caused by medications affecting neurotransmission. This review was prompted by a case of opsoclonus occurring in a patient with Multiple System Atrophy, where amantadine, an NMDA-receptor antagonist, appeared to induce opsoclonus.
UNASSIGNED: Case report of a single patient and systematized review of toxic/drug-induced opsoclonus, selecting articles based on predefined criteria and assessing the quality of included studies.
UNASSIGNED: The review included 30 articles encompassing 158 cases of toxic/drug-induced opsoclonus. 74% of cases were attributed to bark scorpion poisoning, followed by 9% of cases associated with chlordecone intoxication. The remaining cases were due to various toxics/drugs, highlighting the involvement of various neurotransmitters, including acetylcholine, glutamate, GABA, dopamine, glycine, and sodium channels, in the development of opsoclonus.
UNASSIGNED: Toxic/drug-induced opsoclonus is very rare. The diversity of toxics/drugs impacting different neurotransmitter systems makes it challenging to define a unifying mechanism, given the intricate neuronal pathways underlying eye movement physiology and opsoclonus pathophysiology.

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BACKGROUND: Trauma-induced orbital blowout fracture (OBF) with eyeball displacement into the maxillary sinus is rare.
METHODS: We present the case of a 14-year-old with a closed head injury, OBF, and displacement of the eyeball into the maxillary sinus following a car accident. A prompt transconjunctival access surgery was performed for eyeball repositioning and orbital reconstruction in a single session, mitigating anaesthesia-related risks associated with multiple surgeries. At the 12-month follow-up, his visual acuity was 20/200. Despite limited eye movement and optic nerve atrophy, overall satisfaction with the ocular appearance was achieved.
CONCLUSIONS: This report offers novel insights into the mechanisms of OBF occurrence and the development of postoperative complications.

BACKGROUND Pseudo-Brown syndrome is characterized by dysfunction of the superior oblique tendon-trochlear complex. Canine tooth syndrome, which involves superior oblique palsy with pseudo-Brown syndrome, results from damage to the trochlear and superior oblique tendon from dog bites around the eye. This report describes a variant of canine tooth syndrome without pseudo-Brown syndrome following a dog bite around the left upper eyelid. In this case, magnetic resonance imaging (MRI) facilitated early diagnosis and therapeutic intervention. CASE REPORT A 19-year-old man presented with torsional diplopia following a dog bite around the left upper eyelid and forehead. Five days after the injury, an alternate prism cover test revealed 6 prism diopters (Δ) exotropia and 5Δ left hypertropia. Ocular motility showed no significant limitation in elevation or depression during adduction. MRI performed on the same day showed a high-signal area extending from the superior oblique tendon to the trochlear region and the superior oblique muscle belly of the left eye. A diagnosis of canine tooth syndrome without pseudo-Brown syndrome was made and oral steroids were administered. Ocular alignment did not improve, so left inferior oblique myotomy was performed 7 months after the injury. The patient\'s cyclovertical diplopia resolved postoperatively. CONCLUSIONS Dog bites around the eye can result in abnormalities of the extraocular muscles. Early MRI may be useful for diagnosis and determining treatment strategies. This report has highlighted the importance of rapid assessment and management of patients with dog bites involving the eye.

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Opsoclonus-myoclonus-ataxia syndrome (OMAS) is an autoimmune central nervous system disorder, primarily manifesting as a paraneoplastic sequalae to neuroblastoma, and characterized by motor disorders and behavioral disturbances. OMAS is typified by aberrant B-cell and T-cell activation. Current treatment involves immunosuppression using corticosteroids, intravenous immunoglobulin, and rituximab. However, these approaches often lead to treatment-related toxicities and symptomatic recurrences with chronic neurocognitive impairment. We treated three children with refractory neuroblastoma-associated OMAS with tacrolimus, a T-cell-targeting calcineurin inhibitor, effectively controlling symptoms within a month and enabling the discontinuation of immunosuppression with minimal side effects. Tacrolimus shows promise as a therapeutic option for refractory OMAS.