Positron emission tomography

From Ganfyd

See pre-eclampsia for pre-eclampsia toxaemia.

Positron emission tomography is an imaging technique that maps tissue metabolism to anatomical detail. A radioactive isotope is incorporated into a tracer compound and is administered intravenously. For instance, 18-fluorine is commonly given as 18-fluorodeoxyglucose (FDG). Positrons (anti-electrons) from the tracer isotope annihilate with an electron in the patient.

Two photons of electromagnetic radiation, at characteristic energies, are emitted in opposite directions. An array of (scintillation) detectors surrounding or encircling the volume of interest will usually detect both photons, at exactly (for sensible values of "exact") the same time. After this has happened sufficiently many times, the resulting data is analysed and processed to construct an image of the space they came from, i.e. the process of tomography.^[1]

Applications

The tracer is taken up differently by different tissues. Areas of high metabolism take up more glucose and result in a higher signal. This is useful in detecting, for instance, micrometastases that are not visible on conventional imaging.

The reverse is true. Areas of low metabolism can be detected as a relatively weak signal. This property is exploited in cardiac PET scanning which gives an idea of whether the heart muscle is dead, hibernating or well-perfused.

It can also be used to study brain metabolism.

PET gives poor anatomical tissue detail. For instance, it may be difficult to tell if a hot spot is in the mediastinum or in the lung. The usefulness of PET can be enhanced by combining PET and CT. The use of dual modalities allows excellent tissue detail from the CT to be super-imposed on the metabolic picture from PET.

Two image slices from a cardic PET scan

Specific Ligands

• Tissue glucose metabolism
  • ¹⁸F-FDG - ¹⁸F-fluorodeoxyglucose
    • Tumours tend to have high glucose metabolism so micro metastates easily picked up
    • Decreased glucose metabolism in dementia exhibiting the characteristic distributions (but having big overlap) eg
      • Alzheimer's disease Tends to temporal lobe hypometabolism
      • Occipital metabolic loss more proportionately in Dementia with Lewy Bodies than in Alzheimer's disease.
      • Pre-clinical Alzheimer's disease has decreased uptake in the pre-parietal areas
• Cerebral amyloid
  • Naphthyls
    • ¹⁸F-FDDND
  • Thiofavins
    • ¹¹C-PIC - labeling the histological dye usaed for βamyloid !
      • 2-2.5 fold increase in Alzheimer's disease^[2]
    • ¹³¹I -IMPY
  • Stilbenes
    • ¹¹-SB-B
• Parkinsonism
  • ¹¹C-DTBZ)¹¹C-dihydrotetrabenazine
  • ¹⁸F-FP-CIT -¹⁸F 2beta-carbometoxy-3beta-(4-iodophenyl)-N-(3-fluoropropyl) nortropane
    • Distinguish dementia with Lewy bodies from Alzheimer's disease^[3]

References