Posters

Presenting Author

William Reckley MD

Presenting Author Academic/Professional Position

Resident

Academic Level (Author 1)

Resident

Discipline/Specialty (Author 1)

Internal Medicine

Academic Level (Author 2)

Resident

Discipline/Specialty (Author 2)

Neurology

Academic Level (Author 3)

Resident

Discipline/Specialty (Author 3)

Internal Medicine

Academic Level (Author 4)

Faculty

Discipline/Specialty (Author 4)

Neurology

Presentation Type

Poster

Discipline Track

Clinical Science

Abstract Type

Case Report

Abstract

Background: Optic neuritis is a common neuro-ophthalmic emergency and may be the first clinical manifestation of inflammatory demyelinating disease. In the acute setting, clinicians must rapidly distinguish multiple sclerosis (MS) from important mimics, particularly when optic nerve involvement is accompanied by spinal cord lesions. A structured approach integrating phenotype, MRI lesion distribution and activity, and cerebrospinal fluid (CSF) markers can support timely diagnosis and guide counseling regarding long-term management. We report a young man presenting with unilateral optic neuritis and prior transient neurologic episodes, highlighting a practical diagnostic framework applicable to emergency and inpatient care.

Case Presentation: A 27-year-old man with no significant medical history presented with two days of progressive dimming of vision in the left eye with central scotoma and pain worsened by eye movement, in addition to mild left body side deficit. He denied prior visual symptoms. Over the preceding year, he had two self-limited episodes: right arm paresthesias with mild weakness lasting 1 month and, six months later, left leg paresthesias/weakness lasting 3–4 weeks, both with full recovery and no prior evaluation. Stroke code was activated on the emergency department. Examination showed a left relative afferent pupillary defect and diffuse hyperreflexia without focal weakness or gait abnormality. MRI brain demonstrated >20 juxtacortical, periventricular, callosal, brainstem, and cerebellar lesions, with enhancing left insular and parietotemporal lesions including open-ring enhancement. Orbital MRI showed enhancement of the intraorbital and prechiasmatic left optic nerve. Spine MRI revealed cervical and thoracic cord hyperintense lesions. CSF showed elevated IgG index/synthesis and CSF-restricted oligoclonal bands. He improved after intravenous methylprednisolone and was discharged on an oral prednisone taper and vitamin D.

Conclusions: This case demonstrates a stepwise diagnostic approach to optic neuritis that prioritizes (1) confirmation of a typical optic neuritis phenotype, (2) MRI assessment for dissemination in space and activity, and (3) CSF evidence of intrathecal inflammation; in addition to clinical suspicion of underlying inflammatory neurological condition as the patient did not any stroke risk factors present. The widespread brain lesion distribution, coexistence of enhancing and non-enhancing lesions, optic nerve enhancement, and supportive CSF findings favored MS using contemporary diagnostic standards. Optic neuritis with a spinal cord lesion should prompt deliberate evaluation for NMOSD and MOG antibody–associated disease; negative aquaporin-4 testing and the overall clinicoradiologic profile supported MS, while limited MOG testing availability represents a practical constraint to acknowledge. The open-ring enhancement pattern provided an additional imaging clue consistent with demyelination. High-dose intravenous corticosteroids led to symptomatic improvement, consistent with established acute management aimed at accelerating recovery. In patients presenting through emergency pathways, combining clinical phenotyping with targeted MRI and CSF interpretation can expedite accurate diagnosis, avoid misclassification, and enable timely planning for long-term therapy and follow-up.

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Seeing the Pattern: Optic Neuritis, Multifocal MRI Lesions, and the Early Diagnosis of Multiple Sclerosis

Background: Optic neuritis is a common neuro-ophthalmic emergency and may be the first clinical manifestation of inflammatory demyelinating disease. In the acute setting, clinicians must rapidly distinguish multiple sclerosis (MS) from important mimics, particularly when optic nerve involvement is accompanied by spinal cord lesions. A structured approach integrating phenotype, MRI lesion distribution and activity, and cerebrospinal fluid (CSF) markers can support timely diagnosis and guide counseling regarding long-term management. We report a young man presenting with unilateral optic neuritis and prior transient neurologic episodes, highlighting a practical diagnostic framework applicable to emergency and inpatient care.

Case Presentation: A 27-year-old man with no significant medical history presented with two days of progressive dimming of vision in the left eye with central scotoma and pain worsened by eye movement, in addition to mild left body side deficit. He denied prior visual symptoms. Over the preceding year, he had two self-limited episodes: right arm paresthesias with mild weakness lasting 1 month and, six months later, left leg paresthesias/weakness lasting 3–4 weeks, both with full recovery and no prior evaluation. Stroke code was activated on the emergency department. Examination showed a left relative afferent pupillary defect and diffuse hyperreflexia without focal weakness or gait abnormality. MRI brain demonstrated >20 juxtacortical, periventricular, callosal, brainstem, and cerebellar lesions, with enhancing left insular and parietotemporal lesions including open-ring enhancement. Orbital MRI showed enhancement of the intraorbital and prechiasmatic left optic nerve. Spine MRI revealed cervical and thoracic cord hyperintense lesions. CSF showed elevated IgG index/synthesis and CSF-restricted oligoclonal bands. He improved after intravenous methylprednisolone and was discharged on an oral prednisone taper and vitamin D.

Conclusions: This case demonstrates a stepwise diagnostic approach to optic neuritis that prioritizes (1) confirmation of a typical optic neuritis phenotype, (2) MRI assessment for dissemination in space and activity, and (3) CSF evidence of intrathecal inflammation; in addition to clinical suspicion of underlying inflammatory neurological condition as the patient did not any stroke risk factors present. The widespread brain lesion distribution, coexistence of enhancing and non-enhancing lesions, optic nerve enhancement, and supportive CSF findings favored MS using contemporary diagnostic standards. Optic neuritis with a spinal cord lesion should prompt deliberate evaluation for NMOSD and MOG antibody–associated disease; negative aquaporin-4 testing and the overall clinicoradiologic profile supported MS, while limited MOG testing availability represents a practical constraint to acknowledge. The open-ring enhancement pattern provided an additional imaging clue consistent with demyelination. High-dose intravenous corticosteroids led to symptomatic improvement, consistent with established acute management aimed at accelerating recovery. In patients presenting through emergency pathways, combining clinical phenotyping with targeted MRI and CSF interpretation can expedite accurate diagnosis, avoid misclassification, and enable timely planning for long-term therapy and follow-up.

 

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