▶️Initial non-con CT shows a 3cm hyperdense lobulated extra-axial mass in the expected region of the left MCA bifurcation, consistent with a giant aneurysm. There are associated peripheral calcifications
▶️ What is the cause of the surrounding hypodensity?
What is the cause for the surrounding hypodensity?
▶️Mass effect and/leakage from the aneurysm induces vasogenic edema which moves easily through the white matter and relatively spares the more dense gray matter.
▶️However, we also see more subtle hypodensity of the lateral temporal lobe cortex, suspicious for acute ischemia
▶️CTA shows filling of the partially thrombosed aneurysm
▶️CT perfusion shows reduced CBF and corresponding elevated Tmax within the left MCA territory
▶️I am not sure if the stroke is due to thromboembolism from intraaneurysmal thrombus or if it’s 2/2 altered flow kinetics given the large size 🤷🏻♂️ (no occlusion was seen)
▶️Thoughts welcome 🙏
▶️MR shows the hypointense aneurysm on T2 with mixed iso and hyperintensity on T1
▶️ADC nicely delineates the areas of shine through from vasogenic edema and low ADC value from cytotoxic edema 2/2 infarct
▶️The aneurysm was treated with flow diversion using a pipeline shield rather than coiling due to a wide neck.
▶️Follow up, shows persistent filling of the sac despite stent placement
Learning points:
💡 Most intracranial aneurysms are asymptomatic
💡 Complications include rupture and rarely stroke
💡 When you see vasogenic edema around an aneurysm you must worry about impending rupture/leaking (as shown below, 24 hours apart in a different patient)
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🔷False cords (vestibular folds): Basically an inferior reflection of the aryepiglottic fold around the vestibular ligament
🔷Finding the false cords: Since the false cords have an attachment to the top of the arytenoid cartilage and are surrounded by paraglottic FAT we look for the TOP of the ARYTENOID cartilage and FAT in the same plane
🔷True vocal cords (vocal folds): Thickened free superior border of the conus elasticus forms the vocal ligament which is the structure of the true cord. The vocalis & thyroarytenoid MUSCLES release tension on the cord.
🔷Finding the true cords: Look for MUSCLE density and NO paraglottic fat at the level of the CRICOARYTENOID JOINT
⭐️ Answer: Spontaneous spinal epidural hematoma (no clear risk factor in this case)
🔷CLINICAL: Abrupt onset of severe neck or back pain that can radiate into the extremities and commonly is followed by symptoms ranging from nerve root agitation to full neurologic impairment
🔷RISK FACTORS:
▶️Idiopathic (40-60%)
▶️Anticoagulant use
▶️AVM, AVF or other vascular malformation
▶️Underlying coagulopathy
▶️Tumor
▶️Pregnancy
❓ Possible explanation for cases without known risk factors: 🧠 🩸The internal epidural plexus that drains the abdomen and thorax is a low pressure, valveless system that may rupture when the pressure is increased from valsalva maneuvers ❓
🔷For glioblastoma we need to rely on many clinical and imaging features to distinguish (no one feature is specific enough to diagnose so we need to take the whole clinical and radiographic picture into account)
🔷Important features to consider:
▶️Recency of treatment
💡 Radiation necrosis is usually seen from 2 to 32 months after therapy, with 85% of cases occurring within 2 years. A new or worsening abnormality starting 3 years after completion of radiation therapy is very unlikely to be due to pure radiation necrosis. In the first 2–3 years, both tumor and radiation necrosis can occur
▶️Clinical symptoms (although both tumor progression and radiation necrosis can be symptomatic, we want to be careful calling tumor progression in a patient who is clinically doing well as this is devastating news for the patient and there are only limited options for therapy)
⭐️ Answer: petrous apicitis complicated by brainstem abscess
🔷Petrous apicitis can display the clinical triad of Gradenigo’s syndrome
1️⃣Otorrhea
2️⃣Cranial nerve 6 palsy
3️⃣Pain in distribution of trigeminal nerve
▶️Petrous apicitis usually occurs as a complication of otomastoiditis when the infection spreads to the skull base.
▶️The petrous apex is in close proximity to Dorello’s canal (where cranial nerve 6 runs through) and Meckel’s cave (where the trigeminal ganglion is located)
▶️CVT causes retrograde venous pressure leading to focal vasogenic edema
▶️Increased back pressure is characterized by dilated veins and petechial hemorrhage which can progress to large hematomas and ischemic neurological damage
🔷Two types of edema can develop:
1️⃣Vasogenic (from venous back pressure)
2️⃣Cytotoxic (ischemia)
🔷Risk factors:
💡 Up to 20% are idiopathic
1️⃣Trauma
2️⃣Tumor/malignancy (compression/invasion from meningioma)
3️⃣Infection
4️⃣Hormonal (pregnancy)
5️⃣Dehydration