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Introduction The nuclei in the periaqueductal gray of the midbrain are critical structures that coordinate and control vertical and torsional gaze, as well as crucial components of the vestibulo‐occular reflex. These structures are so fine that they may be missed on routine imaging however, they represent distinct localizations for the neurological exam, with lesions of these structures being important clinical considerations. The Interstitial Nucleus of Cajal (inC) coordinates signals from the saccadic burst neurons in the rostral interstitial nucleus of the medial longitudinal fasiculus (riMLF), vestibular projections (utricular and semicircular canal pathways from the vestibular nuclei via the MLF), and descending pursuit fibers, the paired interstitial nuclei of Cajal act as neural integrators for vertical gaze and torsion. These nuclei lie adjacent but dorsal and caudal to the riMLF, For upgaze, fibers from the inC cross via the posterior commissure, then connect to the contralateral superior rectus and inferior oblique subnuclei. For downgaze, fibers travel across the posterior commissure, then innervate the contralateral inferior rectus subnucleus and fourth nerve nucleus. Blood supply is derived from the terminal branches of the basilar artery. Lesions of these interstitial nuclei and their tracts may produce vertical and torsional gaze‐holding deficits such as impairments in the vertical vestibulo‐occular reflex, hypertropia, counter‐rolling of the eyes, superior oblique palsy, and see‐saw and torsional nystagmus. Methods Case report and review of literature Results 45‐year‐old, right‐handed woman with history of turner syndrome, anemia, nephrolithiasis, horseshoe kidney, premature ovarian failure on hormone replacement therapy (HRT), suspected adrenal mass of undetermined significant, and degenerative disk disease presented to the emergency department with complaints of acute binocular diplopia and dizziness clarified to be sensation of the ground/objects bobbing in visual field. Neurological exam significant for left hypertropia and exotropia in primary gaze, equal in right/left gaze and right/left head tilt, as well as large amplitude medium frequency (see‐saw) nystagmus characterized by upbeat nystagmus with intorsion on the right, and downbeat nystagmus with extorsion left. Visual fields were intact to finger count with binocular diplopia and oscillopsia noted in primary gaze. CT head and CT angiogram of the head and neck were unrevealing. Initial MRI brain negative for diffusion restriction but with flair hyperintensity in periaqueductal gray prompting repeat MRI brain without contrast with thin slices through the brainstem with showed infarct in periaqueductal gray within the region of the interstitial nuclei, with stroke etiology undetermined at the time of presentation but suspicion of small vessel disease vs hypercoagulability given propensity for thrombophilia in Turner syndrome and patient being on HRT. Full dose aspirin and high intensity statin therapy was initiated given presentation out of tPA window, and hypercoagulability workup initiated prior to discharge. Conclusion Acute ischemic stroke and lesions of the interstitial nuclei in the periaqueductal gray are important, under recognized considerations for the evaluation of binocular diplopia, that may represent an opportunity for thrombolytic administration if providers had a higher index of suspicion. Hypercoagulability and Turner syndrome are also unique qualifiers, underscoring a nuanced approach to determination of stroke diagnosis and etiology in cases of isolated ocular symptomology.

Introduction Spinal cord infarctions (SCI) are scarce entities, constituting only 0.3‐1% of all strokes, with complete or posterior spinal cord involvement detailed in the case below being even rarer. Often caused by sudden interruption of blood flow to the spinal cord due to embolic phenomena, intrinsic factors such as connective tissue disease, and due to intra/post‐operative hypotension leading to ischemia or infarction. The resultant acute spinal cord dysfunction manifests as; motor weakness, loss of senses of pain and temperature, altered proprioception, bowel and bladder dysfunction Spinal blood supply comprises of the anterior spinal artery (ASA) and the two posterior spinal arteries, with supply to the spinal arteries being derived from various regional arteries: C1‐T3 is supplied by the vertebral arteries, T3‐T7 is served by a branch from the intercostal arteries, and the Adamkiewicz artery supplies T8 to the medullary conus. The thoracolumbar level is primarily supplied by only a small number of radicular arteries, originating from segmental branches of the aorta, specifically the posterior intercostal and lumbar branches, which extend towards the intervertebral foramina where they split into the anterior and posterior radicular arteries. The largest radicular artery, commonly referred to as the arteria radicularis magna of Adamkiewicz (or main anterior radicular artery), typically arises on the left between T9 and T12, but may be located on the right or emerge anywhere from T5 to L4 in approximately 17% of cases. This extensive segment of the spinal cord only is typically supplied by only two or three small radicular branches, occuring between the lower cervical and mid‐to‐lower thoracic levels, making it a watershed zone. Methods Case report and literature review Results 73‐year‐old woman with history of hypertension, long‐term smoking, extensive peripheral vascular disease, R lung cancer (in remission after 3 rounds of radiation, and newly diagnosed calcified heterogeneous left renal mass concerning for malignancy status‐post right femoral access with embolization of left lumbar arteries at the level of L1‐L3 with 800 micrometer particles and tungsten‐platinum coils on 12/19/22), transferred from a surgical center on 12/21/22 for post‐operative paraparesis (R›L), paresthesia , urinary retention, and constipation initially thought to be post‐anesthetic effects. MRI T and L spine with and without contrast demonstrated diffusion restriction from the level of T10 to the conus suggestive of anterior and posterior spinal cord infarct, thought to be in the setting of recent embolization with extensive atherosclerotic burden. Neurological exam significant for lower extremity paraparesis ( R 2/5 , L 3/5) with T10 sensory level to pin‐prick and temperature, hyporeflexia, and absent proprioception in bilateral lower extremities. Full dose aspirin and high intensity statin was started with patient managed conservatively due to presentation outside window for thrombolysis. Conclusion Spinal cord infarcts typically present with motor weakness due to ASA occlusion however, sensory level and proprioceptive loss as accompanying factors are important considerations to rule in total cord (anterior + posterior) infarcts, especially in post‐op patients undergoing thoraco‐lumbar access/embolization as earlier recognition may make them eligible for treatments such as thrombolysis.

Introduction Dolichoectasia is a term used to describe dilated, elongated and tortuous arteries due to defects within the medial layer of their walls secondary to loss of elasticity. Multiple pathophysiological processes might lead to the development of dolichoectatic vessels, and activation of metalloproteinases and irregular turbulent blood flow seem to cause irreversible disruption of the internal elastic lamina. Consequences often include mass effects and ischemic and hemorrhagic stroke. Blood flow within dolichoectatic arteries is turbulent predisposing to thrombus formation with resultant ischemic strokes. Ideally, with optimal anticoagulation therapy, such strokes can be prevented. However, in rare instances, they can still occur despite anticoagulation, likely due to direct compression of pontine perforators from dolichoectasias or persistent turbulent flow. Methods Case report Results A 66‐year‐old woman with hypertension, diabetes mellitus, atrial fibrillation (taking warfarin at home), and left‐sided trigeminal neuralgia due to compressive left vertebrobasilar dolichoectasia with a focal fusiform aneurysm, presented with transient dysarthria and lightheadedness lasting for less than an hour. MRI brain did not show any acute pathology. CTA head showed worsening left vertebrobasilar dolichoectasia with transitional fusiform aneurysm (24 mm in diameter) with mass effect on the anterior part of the pons and lower midbrain. Next day, the patient developed dysarthria and right‐sided weakness, and a repeat MRI brain showed a left acute paramedian pontine infarct. Warfarin was discontinued, and the patient was started on a heparin drip and later transitioned to Apixaban. Eventually, a diagnostic cerebral angiogram and surpass stent placement within the aneurysm were attempted which went uneventful and the flow through the aneurysm regularized. The patient was eventually discharged home on Apixaban and Prasugrel with interval follow‐up. Conclusions Compression of perforating vessels supplying brainstem structures, branching off the pathologic vertebrobasilar dolichoectasia is a rare etiology of acute pontine ischemic stroke, not with standing the anticoagulation. It warrants immediate neurosurgical intervention to optimize blood flow and prevent a recurrence.