Originate in the subpial astrocytes typically in children and young adults often with a seizure history
Temporal lobe is most common
Imaging (variable):
▶️Classically appear as a cortically based mass with cyst and enhancing nodule and overlying DURAL TAIL or enhancing leptomeninges
▶️Calcifications are RARE
▶️Can look very similar to ganglioglioma though calcifications are rare in PXA and if you’re lucky enough to have a dural tail/enhancing leptomeninges then PXA is favored
▶️Companion case of another PXA below
2️⃣DNET
▶️Cortically based mass in children and young adults presenting with long-standing seizures
▶️Most frequently occurs in temporal and frontal lobes
Imaging:
▶️Classically presents as a well demarcated cortically based “BUBBLY” mass with HYPERINTENSE RIM AROUND CYSTS ON FLAIR
▶️Usually there is NO ENHANCEMENT (though can have punctate or ring enhancement). However, when enhancement is seen, consider the possibility of more aggressive tumors.
▶️Companion case below of another DNET
3️⃣Oligodendroglioma
▶️Cortically based mass mainly in ADULTS
▶️Location: FRONTAL and temporal lobes most common
Imaging:
▶️Classically presents as a gyriform cortical/subcortical based mass with GYRIFORM OR CLUMPED CALCIFICATIONS
▶️Consider this diagnosis in an ADULT WITH A CALCIFIED FRONTAL MASS
4️⃣Ganglioglioma
▶️Occurs in children and young adults
▶️Location: Temporal lobe (most common)
Imaging (variable and can look very similar to PXA):
▶️Classically presents as a cystic and solid mass in the temporal lobe in a child/young adult with seizures
▶️Presence of CALCIFICATIONS & LACK OF DURAL TAIL may help to differentiate from PXA
Companion case of another ganglioglioma
💡 Learning points/summary:
P-DOG 🐶
1️⃣PXA: Cyst w/ enhancing mural nodule with DURAL TAIL/leptomeningeal enhancement and NO CALCIFICATIONS
2️⃣DNET: BUBBLY well demarcated mass with NO ENHANCEMENT
3️⃣Oligodendroglioma: Gyriform mass in frontal lobe of an ADULT w/ CALCIFICATIONS
4️⃣Ganglioglioma: Cyst w/ enhancing nodule in temporal lobe w/ CALCIFICATIONS and NO DURAL TAIL
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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