Internal Carotid Artery Dissection Presenting with Transient or Subclinical Horner Syndrome.

Introduction: The most frequently encountered symptoms in internal carotid artery dissection (ICAD) are head or neck pain and cerebral ischemia. Ocular symptoms or signs have been reported as the presenting feature in up to 50% of patients, with (painful) Horner syndrome being the most frequently associated. Horner syndrome is part of the classic triad that depicts the characteristic presentation of ICAD and that consists of pain in the ipsilateral neck, head and orbital regions, (partial) Horner syndrome, and cerebral or retinal ischemia. All patients presenting with painful Horner syndrome should therefore require prompt investigations to rule out carotid artery dissection. In patients with confirmed diagnosis, treatment should be started early to prevent permanent ocular or cerebral complications. Case Presentation: Case 1: A 61-year-old woman presented with right temporal headache, an episode of transient visual loss and drooping of the right upper eyelid. Examination revealed anisocoria, which was more important in darkness. Reversal of anisocoria was observed after instilling drops of apraclonidine 0.5%. Neuroimaging demonstrated intrapetrous ICAD. Headaches, eyelid ptosis, and anisocoria all had resolved the next day. Apraclonidine pharmacologic testing a few weeks later was no longer dilating the previously smaller pupil. Case 2: A 48-year-old man presented with drooping of the right upper eyelid and right occipital headache and facial pain that all started one day after an intense yoga workout. Anisocoria was noticed upon examination, with topical cocaine 10% pharmacologic testing confirming a right Horner syndrome. Neuroimaging revealed ICAD. The patient reported resolution of his eyelid ptosis a few days later. Eyelid ptosis and anisocoria had indeed resolved at a follow-up examination a few weeks later. However, cocaine drop testing still produced anisocoria, compatible with subclinical Horner syndrome. Conclusion: Transient or subclinical Horner syndrome can be the presenting feature in ICAD; in such cases, the characteristic eyelid ptosis and anisocoria may be short-lived and resolve in only a few days. If suspected by clinical history, pharmacologic testing may be helpful in identifying subclinical cases.

Sarcoidosis revealed by simultaneous optic nerve and eyelid involvement: A case report.

PURPOSE: Ocular disease can be the initial manifestation in patients with sarcoidosis. It is most often associated with uveitis, but eyelid or optic nerve disease can also be presenting features. Although uncommon and easy to overlook in a patient presenting with visual loss, paying attention to the presence of eyelid granulomas in our patient proved to be very helpful in our diagnostic work up for optic neuropathy. OBSERVATIONS: A young otherwise healthy patient was addressed with a 3 month history of bilateral painless visual loss. At presentation, best-corrected visual acuity was counting fingers in both eyes. Anterior segment slit-lamp examination was completely normal in both eyes. Eye fundus examination revealed subtle optic disc swelling in the left eye. Interestingly, flesh-colored nodular eyelid lesions were found bilaterally. Basic work-up for optic neuropathy showed elevated levels of serum lysozyme and serum angiotensin converting enzyme. More importantly, a biopsy specimen of an eyelid nodule demonstrated multiple non-necrotizing granulomas, a hallmark sign of sarcoidosis. Despite a delay in treatment of several months after onset of symptoms, response to systemic corticosteroids was prompt and important with visual acuity improving to 20/20 in both eyes as well as complete resorption of all eyelid lesions. CONCLUSION AND IMPORTANCE: In the diagnostic work-up for optic neuropathy, the answer can sometimes be hiding where it's least expected: the possible presence of eyelid lesions should not be overlooked as they may orient us towards sarcoidosis as an underlying etiology.

Subclinical Choroidal Inflammation Revealed by Indocyanine Green Angiography in Tubulointerstitial Nephritis and Uveitis Syndrome.

PURPOSE: To describe subclinical chorioretinal lesions revealed by indocyanine green angiography (ICGA) and their evolution under systemic treatment in tubulointerstitial nephritis and uveitis (TINU) patients. METHODS: Retrospective case series of three patients with TINU syndrome. Choroidal and retinal involvement were assessed by fluorescein angiography (FA) and ICGA. RESULTS: Three patients were analyzed. FA demonstrated hot disc, associated in two cases with retinal vascular leakage, and ICGA revealed subclinical chorioretinal dots in all three cases. Given the presence of posterior uveitis and deterioration of kidney function, asystemic treatment by oral methylprednisolone was started. Persistence of retinal and choroidal inflammations under systemic corticosteroids required association with immunosuppressive agent to control the disease activity. CONCLUSION: Multimodal imaging and more precisely ICGA is useful to assess subclinical choroidal inflammation and monitor treatment response in TINU syndrome. Immunosuppression needs to be revised and adapted when uveitis and/or kidney function are unresponsive to systemic steroids. ABBREVIATIONS: TINU: tubulointerstitial nephritis and uveitis; TIN: tubulointerstitial nephritis; ACE: angiotensin-converting enzyme; RF: rheumatoid factor; Uß2M: urinary ß-2microglobulin; AMPPE: acute multifocal placoid pigment epitheliopathy; FA: fluorescein angiography; ICGA: indocyanine green angiography; CT: computed tomography.

Potential Interplay between Hyperosmolarity and Inflammation on Retinal Pigmented Epithelium in Pathogenesis of Diabetic Retinopathy.

Diabetic retinopathy is a frequent eyesight threatening complication of type 1 and type 2 diabetes. Under physiological conditions, the inner and the outer blood-retinal barriers protect the retina by regulating ion, protein, and water flux into and out of the retina. During diabetic retinopathy, many factors, including inflammation, contribute to the rupture of the inner and/or the outer blood-retinal barrier. This rupture leads the development of macular edema, a foremost cause of sight loss among diabetic patients. Under these conditions, it has been speculated that retinal pigmented epithelial cells, that constitute the outer blood-retinal barrier, may be subjected to hyperosmolar stress resulting from different mechanisms. Herein, we review the possible origins and consequences of hyperosmolar stress on retinal pigmented epithelial cells during diabetic retinopathy, with a special focus on the intimate interplay between inflammation and hyperosmolar stress, as well as the current and forthcoming new pharmacotherapies for the treatment of such condition.