Before being able to pinpoint pathologies, you must first know normal variants. What is that hole doing in the basilar artery? What benign variant is this? #FOAMed

We often talk about the middle cerebral artery (MCA), probably because it's one of the most commonly occluded arteries in ischemic stroke. Why? The MCA is essentially the more direct continuation of the internal carotid artery (ICA), making it a common destination for emboli traveling downstream from the heart or carotid arteries. But what about the anterior cerebral artery (ACA)? Pic 1 is from Radiopaedia.org. Follow the diagram as you read along. What are the symptoms of an ACA occlusion? And should we perform mechanical thrombectomy for these patients? The role of endovascular thrombectomy for isolated proximal ACA occlusion (A1) remains uncertain. Personally, I favor considering thrombectomy when the occlusion is identified early and the neurological deficits are disabling, provided the anatomy and imaging are favorable. The ACA, just like the MCA, has several segments. A1 segment As the ACA leaves the ICA and travels toward the anterior communicating artery (AComm), it's called the A1 segment. The ACA supplies structures involved in neurocognitive functions, including personality, behavior, memory, motivation, and even bladder control. So what happens when these areas are affected by a stroke? Think: • Personality changes, including disinhibition (inappropriate behavior during examination) • Abulia (loss of motivation) • Akinetic mutism (marked reduction in movement and speech) • Urinary incontinence • Contralateral leg weakness, often greater than arm weakness These symptoms can easily be missed or underestimated, particularly when relying on NIHSS alone. A2 segment After the AComm, the ACA becomes the A2 segment, extending toward the genu of the corpus callosum. A2 occlusions are generally classified as medium vessel occlusions (MeVOs), rather than the conventional large vessel occlusions (LVOs) encountered in thrombectomy trials. Should we remove these clots? That depends. Vessel caliber, vascular anatomy, infarct burden, and, importantly, the severity and disabling nature of the neurological deficits should all influence the decision. A larger or dominant ACA branch may supply substantially more territory, potentially resulting in greater neurological deficits. But remember, NIHSS does not adequately capture every disabling manifestation of an ACA stroke. A3 segment As the ACA curves around the genu of the corpus callosum, it becomes the A3 segment. This is also considered a MeVO. Here, making a compelling argument for thrombectomy becomes more difficult. Current randomized evidence has not demonstrated an overall benefit of routine thrombectomy for distal and medium vessel occlusions. However, individual anatomy matters. A relatively large or dominant branch supplying an extensive territory may present a different clinical scenario. And as vessel caliber decreases, endovascular navigation becomes more challenging, with increasing concern for vessel injury, perforation, and subsequent hemorrhage. A4 and A5 segments After the ACA curves around the genu and travels posteriorly along the corpus callosum, we enter the A4 and, more distally, A5 segments. These are smaller, more distal vessels. Routine thrombectomy here is difficult to justify based on current evidence, although exceptional circumstances may warrant individualized consideration. Now that you've had this brief anatomy lesson, let's test your understanding. Look at pic 2. This CTA demonstrates an ACA occlusion. 1. Which ACA segment is occluded? 2. If the NIHSS is <6, what would be your preferred approach to treatment? Bonus question! Before you go, let's see how well you know your cerebrovascular anatomy. I've marked three additional structures with red arrows labeled B, S, and V. Can you identify all three? Here's a hint: One is an artery, and the other two are part of the cerebral venous drainage system. #FOAMed

Is there a connection between this structure, this protuberance, and alcohol? What's the triad? Drop your thoughts below 👇 #FOAMed #Neuroanatomy #Wernicke

Our hands, feet, and eyes are strikingly symmetric in size. Blood vessels? Not always. It’s common for one vertebral artery to be dominant while the other is congenitally hypoplastic. But how do you know that tiny vertebral artery on the left (red arrow) is truly hypoplastic and not diminutive because of proximal atherosclerotic disease or dissection? Here’s a neat anatomical clue: look at the transverse foramen. The vertebral arteries ascend through the transverse foramina of the cervical vertebrae. During development, the vertebral artery and its surrounding bony canal develop in close relationship. Thus, the caliber of the vessel tends to correlate with the size of the transverse foramen: a smaller vertebral artery tends to have a smaller foramen, while a larger vertebral artery tends to have a larger one. So, if you see a tiny vertebral artery with a correspondingly tiny transverse foramen, that’s an important clue that the vessel is congenitally small. A tiny vertebral artery traveling through a much larger transverse foramen, however, should make you consider an acquired diminutive vessel, such as from proximal atherosclerotic disease or dissection. Now compare the two sides. 🟢 The dominant vertebral artery travels through a larger transverse foramen. 🔴 The hypoplastic vertebral artery travels through a correspondingly smaller transverse foramen. That smaller transverse foramen is an important clue that the artery has been small developmentally rather than becoming small later from acquired vascular disease. It’s an anatomical variant. It’s normal. Know normal anatomy before you confidently call pathology. #FOAMed