▶️Low T2 signal (less cytoplasm and more nucleus so less water in cells and lower T2 signal)
▶️Hyperdensity on CT
▶️Periventricular location
Hypercellular tumor continued
▶️Glioblastoma or high grade glioma
Variable but may have more eccentric or nodular restriction around areas of necrosis and heterogeneous enhancement
4️⃣HEMATOMA
RBCs trapped in serum and fibrin can restrict on DWI (though blood can also be dark on DWI from susceptibility)
Hyperdensity on CT is a giveaway but this may fade overtime or you may not have a CT
Look for a rim of HYPERINTENSITY ON T1 and HYPOINTENSITY on SWI
5️⃣DEMYELINATION
High signal on DWI is predominantly due to T2 SHINE THROUGH
True restriction may be seen at the LEADING EDGE (along the margin) in acute demyelination possibly from cytotoxic edema, reduced fiber tract organization, or myelin fragments
(This example is PML)
6️⃣EPIDERMOID CYST
Tightly organized epithelial layers cause a light bulb bright restriction
ADC tends to be ISOINTENSE TO BRAIN PARENCHYMA (not super dark), possibly from movement of fluid between layers (at least that’s how I think of it)
Epidermoid cyst continued
▶️CSF intensity on T1 & T2
▶️Dirty on FLAIR
▶️DO NOT ENHANCE! (May have a tiny rim of enhancement along edge but NO CENTRAL)
Bonus cases
7️⃣SEIZURE
Shows gyriform or cortical restricted diffusion (often in the mesial temporal lobe)
Examples in 2 different patients
8️⃣ENCEPHALITIS
Diffusion restriction in the insula and temporal lobes favors herpes encephalitis, though any encephalitis can cause restriction
Herpes is usually bilateral but asymmetric and may have patchy enhancement and hemorrhage
Case of herpes
9️⃣CJD
Diffusion restriction is seen in the basal ganglia, thalami, and cortex. This can be asymmetric
🔟Many Toxic/metabolic disorders
Hepatic encephalopathy
Acute toxic leukoencephalopathy
Hypoxia
Methotrexate toxicity
Drug abuse
CO poisoning
Many more
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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