Nuclide Notes

☢️ Meningiomatosis ☢️ Planar bone scan shows intense tracer uptake involving a confluence of right skull bones and multifocal areas of variable degrees of uptake in multiple left skull bones. SPECT/CT images show extensive marked hyperostotic expansile sclerosis involving the anterior and middle skull base, marked in the right side corresponding to intense delayed tracer uptake. There is associated extra axial paraosseous plaque like dural ossification along the middle cranial fossa. Features suggestive of meningiomatosis.
🗓 Meningiomatosis refers to multiple separate meningiomas which is uncommon with an incidence of 2-10%. It can be sporadic or associated with genetic syndromes such as NF2. While usually an incidental findings clinical impact depends on size, location, mass effect, edema, venous sinus involvement, and proximity to critical neurovascular structures. On bone scan they appear and intense tracer uptake involving the skull and can be mistaken for fibrous dysplasia, Paget disease, metastases…etc. MRI is the modality of choice for mapping disease burden, assessing growth, and guiding surveillance or treatment planning.

🧬 FDG is trapped because FDG-6-P becomes a metabolic dead end.

After FDG enters the cell and is phosphorylated by hexokinase ⚡, it cannot efficiently continue through glycolysis because the 2-fluoro substitution prevents normal isomerization 🔒. It also does not meaningfully enter glycogen synthesis or the pentose phosphate pathway, because it is a poor substrate for those enzymes 🚫.

So the signal we see on PET is not just “glucose use” — it is the result of transport, phosphorylation, impaired downstream metabolism, and limited dephosphorylation 📈.

Understanding this is essential for interpreting FDG uptake patterns, pitfalls, and tumor biology 🧠🩻.

More detailed FDG PET/CT concepts are explained in the PET/CT course on BCV Nuclear Medicine Academy 🎓.

🔗 http://bcv.app/nucmed