Our patient is a 70-year-old man with a PMH of anxiety, depression, GERD, and mitral valve repair. He was in usual state of health on the night prior going to bed at 3 am. The next morning he awoke at 9 am with left eye vision loss except for a small crescent of vision in his central vision. He denied eye pain, headache, trauma. He denied temporal artery tenderness, headaches, or jaw claudication. No prior history of glaucoma. Emergent ophthalmologic and stroke neurology consultation confirmed a diagnosis of left Central Retinal Artery Occlusion (CRAO) with macular sparing (Fig 1A-Fundoscopic OS Pre-tPA). Emergent consultation for interventional therapy was requested. 

NEURO-INTERVENTIONAL THERAPY AND HYPERBARIC OXYGEN THERAPY
Dr. Sundeep Mangla performed emergent angiography of the left internal carotid artery and left ophthalmic artery, demonstrating normal origin of the ophthalmic artery with a poor choroidal blush confirming the diagnosis of retinal ischemia (Figure 2, A+B). Superselective angiography of the ophthalmic artery was performed followed by intra-arterial infusion of tPA at a concentration of 0.4 mg/cc for a total dose of 4 mg over 5-7 minutes. The patient reported significantly improved vision immediately after IA tPA therapy, with persistent lateral field cut. The patient then received post interventional hyperbaric oxygen therapy (2.0 – 2.6 atmospheres, 90-120 mins duration) for 4 sessions starting within 12 hours of diagnosis and treatment. A follow-up fundoscopic examination demonstrates improved perfusion of the retinal branches (Figure 1A and 1B, immediate and 2 days post fundoscopic). MRI of the brain confirmed an embolic source of the CRAO, with additional small diffusion positive strokes within the left hemisphere. He was discharged home with significantly improved vision in the left eye for continued outpatient therapy and management.
Figure 1A: OS A. CRAO pre tPA 
Figure 1B: OS B. 30 mins post IA tPA demonstrates improved perfusion and branching vessels of retina
SUMMARY AND DISCUSSION
Central Retinal Artery Occlusion (CRAO) represents on neuro-ophthalmologic emergency, which can lead to irreversible retinal damage secondary to ischemia of a terminal vessel (without collaterals). It is characterized by a sudden, unilateral and painless loss of vision. Embolism is the most common cause of CRAO, the major source of which is carotid artery disease. The natural history for spontaneous recovery or improvement with conservative measures (including paracentesis, acetazolamide, anticoagulation and/or antiplatelets) remains poor, ranging from 20-30% for some measures of functional visional improvement. In studies comparing selective thrombolysis with conservative therapy, Schmidt et al. reported 58% of the interventional therapy group compared with 29% of the control group demonstrated partial improvement in visual acuity, with 77% vs. 26% if treated within 6 hours. 1 Additional studies delivering lower doses of tPA within 4 hours of onset published by Aldrich and colleagues demonstrated significant improvement in visual acuity (at least 1 line on the Snellen chart) in 76% of patients receiving intra-arterial therapy versus 33% of patients in the control group. The Interventional group was 13 times more likely to have improvement in visual acuity of 3 lines or more and 4.9 times more likely to have a visual acuity of 20/200 or better. 2 Although limited due to the heterogeneity of the presentations and therapeutic regimens applied, early experiences suggest opportunities for improved outcomes.
Figure 2. A. Left ICA Angiogram CRaO; B. Selective infusion 4 mg tPA; C. Post IA tPA
(OA-Ophthalmic Artery, CRA-Central Retinal Artery, CB-Choroidal Blush, PCA-Posterior Ciliary Artery)
Hyperbaric oxygen therapy (HBOT) has been associated with visual improvement in retrospective studies. 3 HBOT can maintain oxygenation of the retina through the choroidal blood supply, decrease edema and preserve compromised tissue adjacent to ischemic area. Important key factors for improvement include early therapy (<4-12 hours), degree of vessel occlusion, type of vessel occluded and presence of an adequate PaO2 of oxygen. 4

Our patient experienced the most severe form of CRAO with complete vision loss with only light perception. Despite this critical presentation, with a combination of early Neurointerventional therapy with intra-arterial thrombolysis directed to provide primary revascularization and Hyperbaric oxygen therapy to improve collateral and retinal perfusion, he was able to achieve early functional visual improvement of movement, objects, and color in his lateral fields. CRAO represents an ocular emergency with devastating outcomes. Poor outcomes are more commonly observed with delayed presentation, complete vision loss, and conservative management. Early recognition and potential multi-disciplinary treatment plans may offer patients an opportunity for improved functional outcomes and restoration of vision for these ophthalmologic emergencies and impending strokes of the eyes.
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Neuroendovascular Case Study:
 A painful, enlarging mass behind ear of young girl.
The patient is an eleven year old girl who presented with a painful, discolored swelling behind her left ear. She said the swelling had increased noticeably in size over the previous 6 months.

The swollen area, upon physical examination, proved to be a pulsatile mass, with some reddish discoloration. (Fig. 1A) The results of MRI/MRA imaging was consistent with an extra-cranial AVM, with feeders from the anterior and posterior auricular branches. There was suggestion of feeders from branches of the middle meningeal artery.

Selective angiogram confirmed feeders from the anterior and posterior auricular arteries. (Fig. 2A) Super selective embolization was performed of feeders involved in the auricular cascade with penetration into the draining veins, nidus, and distal dedicated feeding arteries. Concurrently, the ear was packed in ice to stop flow to the normal tissue. One-tenth of a cc of non-opacitied NBCA was used to minimize the mass of embolic material and discoloration. This led to the total obliteration of the AVM.

Follow-up, (Fig. 2B) shows obliteration of the AV shunting. Additional angiography is indicated in 6-12 months to confirm obliteration.
Fig. 1A Posterior aspect of Left Ear.
Fig. 1B Two weeks after embolization the inflammation is gone and the shunt gone by Doppler.
Fig. 2A PA view of Left External Carotid Angiogram showing  posterior and anterior Auricular Arteries in ear, helix and scapha feeding with a dominate fistula.
Fig. 2B Total angiographic obliteration of AVM and fistula with sparing of the Helix cascade( as seen on late films)
Key Points:
  1.  Extra-cranial AVMs can become quite active, and can grow with trauma, puberty, or pregnancy.
  2. Normal tissue blood flow is controlled by tissue temperature, whereas pathological shunts seen in AVM’s are fixed. At temperatures below 20C, there is virtually no flow to normal tissue.It is possible to take advantage of this to spare the normal tissue and target the shunts as in this case.
  3. Angiographic follow-up is needed in all AVM treated cases once the non-invasive imaging has been negative for 6-12 months as it is the only way to confirm cure.
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Internal Carotid Artery Stenosis
A 71 year-old woman woke up with numbness and clumsiness of her right hand. Additionally, she complained of difficulty thinking and often felt like she would fall. On neurological examination she had full strength, but in comparative testing the right hand was weaker. Her past medical history was remarkable for arterial hypertension and coronary heart disease with coronary stenting undertaken 12 years ago. The patient was diagnosed with a proximal left internal carotid artery stenosis (CT angiogram). In addition, brain imaging showed subcortical and cortical ischemic changes and increased Tmax on head CT perfusion imaging (Figures 1) further supporting the diagnosis of a symptomatic carotid artery stenosis.
Figure 1: Ischemic cerebral changes are seen in centrum semiovale and left parietal cortex (top row: brain MRI/FLAIR). Cerebral perfusion imaging with increased Tmax in the left hemisphere (CT perfusion; bottom).
The patient was placed on ASA, statin, and antihypertensive medication. On baseline conventional angiogram, there was reduced visualization of intracranial arteries due to a high-grade left internal carotid artery stenosis. Carotid angioplasty and stenting was performed to restore intracranial circulation with excellent radiological and clinical outcome (Figures 2).
Figure 2: 71 year-old woman with symptomatic high-grade stenosis of the proximal left internal carotid artery (ICA) (filling defect market as yellow,* top middle). Pre-operative, reduced filling of the left middle cerebral artery (M) and no filling of the anterior cerebral artery (A) (top left). External carotid artery branches, superficial temporal and middle meningeal arteries filling ahead of the intracranial circulation on cerebral angiogram (left). Carotid angioplasty and stenting (center) with restitution of carotid lumen post-op (bottom middle) and restoration of intracranial flow with visualization of branches of middle and anterior cerebral arteries (right).
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