Brain radiation is a risk factor for the development of meningiomas …this patient subsequently developed multiple meningiomas including this large frontal meningioma
The mass was treated and immediate post op CT shows expected post op change with the resection cavity, some hemorrhage, and pneumocephalus
1 month later the patient presents with worsening headaches so an MRI was ordered to eval for post op infection
It can be tricky teasing out organizing hematoma from purulent material on MR. CT may not be as helpful as hematoma will reduce in density overtime
we see here there are areas of restricted and intermediate diffusivity within the resection cavity which can be from purulence or blood product
Given the patchy intrinsic T1 hyperintensity, we know at least some of this is related to subacute blood
Patchy hypointensity on SWI is also out of proportion to what one would expect from free radical formation along the periphery in abscess, so this is mostly from blood and perhaps foci of pneumocephalus
However, there is too much vasogenic edema and mass effect for a 1 month post op. Post op edema and blood should progressively decrease while an infected cavity would increase
OR confirmed both blood and pus
Learning points:
💡 CLINICAL SIGNS OF INFECTION ARE MOST IMPORTANT
💡 PROGRESSIVE or OUT of proportion vasogenic edema suggests infection (though do NOT forget about possibility of tumor recurrence!)
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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